Intracellular Calcium Changes in Rat Aortic Smooth Muscle Cells in Response to Fluid Flow

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• 作者：Ritu Sharma ; Clare E. Yellowley ; Mete Civelek ; Kristy Ainslie ; Louis Hodgson ; John M. Tarbell and Henry J. Donahue
• 关键词：Shear stress ; Smooth muscle cells ; Intracellular Ca2+ ; Stretch ; activated channels ; Myogenic tone
• 刊名：Annals of Biomedical Engineering
• 出版年：2002
• 出版时间：March 2002
• 年：2002
• 卷：30
• 期：3
• 页码：371-378
• 全文大小：97 KB
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Biomedicine
  Biomedical Engineering
  Biophysics and Biomedical Physics
  Mechanics
  Biochemistry
  
• 出版者：Springer Netherlands
• ISSN：1573-9686

文摘

Vascular smooth muscle cells (VSM) are normally exposed to transmural fluid flow shear stresses, and after vascular injury, blood flow shear stresses are imposed upon them. Since Ca2+ is a ubiquitous intracellular signaling molecule, we examined the effects of fluid flow on intracellular Ca2+ concentration in rat aortic smooth muscle cells to assess VSM responsiveness to shear stress. Cells loaded with fura 2 were exposed to steady flow shear stress levels of 0.5–10.0 dyn/cm2 in a parallel-plate flow chamber. The percentage of cells displaying a rise in cytosolic Ca2+ ion concentration ([Ca2+]_i) increased in response to increasing flow, but there was no effect of flow on the ([Ca2+]_i) amplitude of responding cells. Addition of Gd3+ (10 M) or thapsigargin (50 nM) significantly reduced the percentage of cells responding and the response amplitude, suggesting that influx of Ca2+ through ion channels and release from intracellular stores contribute to the rise in ([Ca2+]_i) in response to flow. The addition of nifedipine (1 or 10 M) or ryanodine (10 M) also significantly reduced the response amplitude, further defining the role of ion channels and intracellular stores in the Ca2+ response. © 2002 Biomedical Engineering Society.PAC2002: 8716Uv, 8719Uv, 8716Dg, 8719Ff